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COMPLEMENT SYSTEM Flashcards

1
Q

Research on complement began in the 1890s, when Jules Bordet at the Institut Pasteur in Paris showed that sheep antiserum to the bacterium Vibrio cholerae caused lysis of the bacteria and that heating the antiserum destroyed its bact eriolytic activity.
 He named those substances as ______ .
 Paul Ehrlich coined the term _________.

A

Alexins

complement

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2
Q

It is named “complement system” because it was first identified as a _____-labile component of serum that “_________ or ________” antibodies in the killing of bacteria.

A

heat

complemented or augment

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3
Q

Complement system

Consists of ______ and ___________ involved in defense against ______ and tissue damage mediated by ________

A

serum and cell surface proteins

pathogens; antibodies

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4
Q

The Complement system is the (minor or major?) effector of ____________________ branch of immune system.

A

Major

cellular and humoral

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5
Q

Complement system

Plays major role in only innate immunity

T/F

A

F

Plays major role in both innate and adaptive immunity

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6
Q

Complement system represents a group of about _____ proteins which augment or complement the immune response.

Most of these proteins are found in ______ or on _______

A

30

serum; cell surfaces.

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7
Q

Complement proteins

Synthesized in _____ as (active or inactive?) precursors and are activated by ________ during their interaction in a ________ manner.

A

liver

Inactive ; proteolysis; sequential

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8
Q

Complement proteins

Also produced by blood ______, tissue ________ and _______ cells of the ______________ and _____________ tract.

A

monocytes

macrophages; epithelial

gastrointestinal and genitourinary

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9
Q

General properties

Present in ______ of all animals but its concentration is maximum in ______ of ——-

A

serum

serum of guinea pig.

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10
Q

General properties

Complement of one species are able to react with antibodies of other species and to the same extent.

T/F

A

F

Complement of one species are able to react with antibodies of other species but not to the same extent.

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11
Q

General properties

C- proteins constitute about ——% of normal serum protein

Are _________.

Are synthesized (slowly or rapidly?) in inflammatory responses – hence are called ________________

A

5

glycoproteins; rapidly

acute phase proteins.

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12
Q

General properties

Heat (stable or labile?) and lost activity at ____0 C for _____ and inactivated.

Immunoglobulins are inactivated at
this temperature.(T/F)

A

Labile

56; 30mins

F

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13
Q

Complement proteins Binds with __________ of immunoglobulns .

A

Fc potion

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14
Q

Three main effects of complement are:

  1. _____ of cells (bacteria, allografts, tumor cells)
  2. Generation of ___________

3.______________: ______ of ______

A

Lysis

mediators of inflammation

Opsonization

enhancement of phagocytosis

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15
Q

Complement functions

Host benefit:
– _________ to enhance phagocytosis
– phagocyte_______ and. ______
–_____ of bacteria and infected cells
– regulation of _____ responses
– clearance of _________
– clearance of ________

A

opsonization

attraction and activation

lysis; antibody

immune complexes

apoptotic cells

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16
Q

Complement functions

• Host detriment:
–__________,__________

A

Inflammation, anaphylaxis

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17
Q

Complement system

 Complement components-
- Components are designated by _____ (E.g. ;___-____) or ______ (E.g. :______)

A

numbers; C1 – C9

letters; Factor D

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18
Q

Complement system

Complement receptors

Located on_________

recognize _____ components)

A

Cell surface

activated

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19
Q

Complement system

Regulatory proteins of complement

-both in ———- and ______

-they inhibit _________ components

A

serum and cell surface

activated

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20
Q

Complement proteins: are proenzymes

T/F

A

T

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21
Q

Complement proteins: are proenzymes that are activated by _________.

A

cleavage

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22
Q

Example:

a = ———- fragment. - _______

b= ______ fragment. - _________

Exception is : _____

a = ____ fragment
b =_____ fragment

A

smaller

Diffusion

larger

remains bound to microbe

C2

Large; small

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23
Q

Complement Pathway
Three pathway of complement activation

Classical pathway:- Is ______ dependent pathway and triggered by formation of _________________ or by binding of the __________ to _________ on the ————

A

antibody

soluble antigen-antibody complex

antibody to the antigen present on the target cell surface.

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24
Q

Complement Pathway
Three pathway of complement activation

Alternative pathway:- Is ______________ pathway stimulated by ________ eg. Bacterial cell surface components.

A

antibody independent

antigen directly

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25
Q

Complement Pathway
Three pathway of complement activation

Lectin Pathway:- Also a ________ pathway but resembles _______ pathway.

A

antibody independent

classical

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26
Q

Stages of complement Activation
Three main stages in the activation of complement by any pathway are

Formation of __________
Formation of ____________
Formation of _____________

A

C3 convertase

C5 convertase

membrane attack complec(MAC)

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27
Q

Stages of complement Activation

The initiation and formation of C3 convertase are (the same or different?) in classical and alternative pathway .

A

different

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28
Q

Stages of complement Activation

These classical and alternative pathways then follow the parralel route to merge at _________ stage and finally generate the ______ by a _____ route

A

C5 convertase

MAC

common

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29
Q

Of these pathways, the ______ and ______ pathways are more important the first time we are infected by a microorganism because ????

A

lectin and the alternative

the antibody required to trigger the classic pathway is not present.

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30
Q

The lectin pathway but not the alternative pathway is a participant in the innate arm of the immune system.

T/F

A

F

The lectin pathway and the alternative pathway are, therefore, participants in the innate arm of the immune system.

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31
Q

All three pathways lead to the production of ____, the central molecule of the complement cascade.

The presence of ____ on the surface of a microbe marks it as ________ and ______ it for ________

A

C3b

C3b

foreign and targets it for destruction.

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32
Q

C3b has two important functions:

(1) It combines with other complement components to generate ________, the enzyme that leads to the production of the ________________

(2) It _______ bacteria because phagocytes have _____________ on their surface.

A

C5 convertase

membrane attack complex

opsonizes

receptors for C3b

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33
Q

C-activation: _____ of C proteins such that they _________________

A

alteration

interact with the next component

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34
Q

C-fixation: ________ of C by __________

A

utilization

Ag-Ab complexes

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35
Q

C-inactivation: ———— (usually by _____) of _______ ___-component resulting in ____________

A

denaturation

Heat

an early C

loss of hemolytic activity

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36
Q

Convertase/esterase: ____ C-protein which acts as a _______ for _________

A

Altered

proteolytic enzyme

another C-component

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37
Q

Classical pathway

•In the classic pathway, ________ activate C1 to form a ______, which cleaves _______________ to form a _______ complex, ___________ split off.

•The ________ is ________, which cleaves _______ molecules into two fragments, _________

•_____forms a complex with ________ producing a new enzyme, ________ (_________), which cleaves ____ to form ____________

•C5b binds to _____ to form a complex that interacts with ________ to produce the _______(___________), which causes cytolysis.

A

antigen–antibody complexes

protease

C2 and C4 ; C4bC2a; C2b and C4a

C4bC2a is C3 convertase

C3; C3a and C3b.

C3b; C4b,2a, ; C5 convertase ; C4b2a3b

C5; C5a and C5b

C6 and C7; C8 and C9; membrane attack complex ; C5b,6,7,8,9

38
Q

Note that generally the “____” fragment continues in the main pathway, whereas the “___” fragment is split off

A

b

a

39
Q

Only Ig___ and Ig___ fix complement.

A

M

G

40
Q

___ molecule of IgM can activate complement

activation by IgG requires __________ IgG molecules.

A

One

two cross-linked

41
Q

Of the IgGs, only Ig___, Ig____, and Ig___ subclasses fix complement; Ig____ does not.

A

G1

G2

G3

G4

42
Q

C1 is bound to a site located in the____ region of the _____ chain.

C1 is composed of _____ proteins, _______________

A

Fc

heavy

three

C1q, C1r, and C1s.

43
Q

C1q is an aggregate of ____ polypeptides that binds to the ____ portion of _____________

 It is multivalent and can ____________ molecules.

A

18

Fc

IgG and IgM.

cross-link several immunoglobulin

44
Q

C1s is a ______ that is cleaved to form ________

A

proenzyme

an active protease.

45
Q

Functions:

C1q

C1r

C1s

A

Binds to antibody that has bound antigen, activates C1r.

Cleaves C1s to activate protease function.

Cleaves C2 and C4.

46
Q

Functions:

C2a
.
C2b

A

Unknown.

Active enzyme of classical pathway; cleaves C3 and C5.

47
Q

Functions:

C3a

C3b

A

Mediates inflammation; anaphylatoxin.

Binds C5 for cleavage by C2b. Binds cell surfaces for opsonization and activation of alternate pathway.

48
Q

Functions

C4a

C4b

A

Mediates inflammation.

Binds C2 for cleavage by C1s. Binds cell surfaces for opsonization

49
Q

Functions

C5a

C5b

A

Mediates inflammation; anaphylatoxin, chemotaxin.

Initiates assembly of the membrane-attack complex (MAC).

50
Q

Functions

C6

C7.

A

Binds C5b, forms acceptor for C7.

Binds C5b6, inserts into membrane, forms acceptor for C8.

51
Q

Functions

C8

C9n

A

Binds C5b67, initiates C9 polymerization.

Polymerizes around C5b678 to form channel that causes cell.

52
Q

Alternative pathway

Antibody (dependent or independent ?) pathway.

A

Independent

53
Q

Alternative pathway

In the alternative pathway, many ___________ substances, e.g., ________,________,_________,______ can initiate the process by binding ________________

•This complex is cleaved by a protease, _________, to produce __________.

•This acts as a _______ to generate more ____.

A

unrelated cell surface

bacterial lipopolysaccharides (endotoxin), fungal cell walls, and viral envelopes,

C3 and factor B.

factor D; C3bBb

C3 convertase; C3b

54
Q

__________ pathways are more important the first time we are infected

A

Alternative

55
Q

Alternative pathway

Usually activated by _________ like ______________

• Other activators include:
1. Complexes containing Ig___
2. Some ___-infected cells (e.g. EBV)
3. Many gram negative and gram positive organisms
4. Parasites – Trypanosomes, Leishmania
5._________
6._________ (agarose)

A

products of micro-organisms like endotoxin

A

virus

Erythrocytes; Carbohydrates

56
Q

Functions

B

Ba

Bb

A

Binds membrane bound C3b. Cleaved by Factor D.

Unknown.

Cleaved form stabilized by P produces C3 convertase.

57
Q

Functions

Factor D

P(Properdin)

A

Cleaves Factor B when bound to C3b.

Binds and stabilizes membrane bound C3bBb.

58
Q

Lectin Pathway

Also known as the ______(________________) Pathway

A

MBL

mannose-binding lectin

59
Q

Lectin Pathway

In the lectin pathway, ___________ binds to the surface of microbes bearing ________

•Binding causes __________(_______________) that ____________ and _________

A

mannose-binding lectin (MBL)

mannan

activation of MASP

MBP-associated serine proteases

cleave C2 and C4 and activate the classic pathway.

60
Q

Lectin Pathway

mannan

A _______ of the ______, _____

A

polymer of the sugar, mannose

61
Q

Lectin Pathway

this process bypasses ___________________ and so is _________________ before __________

A

the antibody-requiring step

protective early in infection

antibody is formed.

62
Q

Membrane attack complex

C5

structurally homologous to _____________

Lacks __________ bond

A

C3 and C4

internal thioester

63
Q

Membrane attack complex

_____ initiates formation of MAC (complex of ____,_____,_____,_____, and ——— )

•C5b binds to ________, recruits ___ and complex ______________ into the membrane.

A

C5

C5b, C6, C7, C8 and multiple C9 molecules

C6, and C7 ; C8; penetrates more deeply

64
Q

Membrane attack complex

C9, a _____-forming molecule with homology to _______.

The complex of C5b678 forms a ____ for C9________ and _________

A

pore

perforin

nidus

binding and polymerization

65
Q

Membrane attack complex

Penetrates membrane bilayers to form ————

Disrupt the ___________, leading to _______ and ——— of susceptible cells

A

pores

osmotic barrier

swelling and lysis

66
Q

Biologic Effects of complement:
1. Opsonization

• ______ and _____

•enhance ________

A

C3b & C1q

phagocytosis

67
Q

Biologic Effects of complement:

Chemotaxis
• ______ and ___________ complex attract neutrophils

• C5a – enhance _________ of ———— to ________

A

C5a and C5,6,7

adhesiveness of neutrophils to the
endothelium

68
Q

Biologic Effects of complement:

Anaphylatoxin

•_______________
• Cause _______ of ________ cells
• Bind directly to ______ of ________, leading to ________

A

C3a,C4a,C5a

degranulation of mast

smooth muscles

bronchioles

bronchospasm

69
Q

Opsonization increases phagocytosis by _______ fold

A

1,000

70
Q

Biologic Effects of complement:

Cytolysis

•_________
• Disrupt the ______ & the ______________________ into the cell

A

MAC

membrane

entry of water and electrolytes

71
Q

Biologic Effects of complement:

Enhancement of antibody production

• Binding of ____ to its receptors on the surface of activated B cells leads to enhanced antibody production

A

C3b

72
Q

Regulation of Complement System

  1. C1inhibitor

• Important regulator of ____ pathway
• A ___________ (serpin)
• (Reversibly or Irreversibly?) binds to and inactivates ____ and ____, as well as _____ in lectin pathway

A

classic

serine protease inhibitor

Irreversibly

C1r ; C1s

MASP

73
Q

Regulation of Complement System

FactorH
• Regulate ______ pathway
• Reduce amount of ________ available
•With both cofactor activity for the factor I-
mediated C3b cleavage, and decay accelerating activity against C3bBb (C3 convertase)

A

alternative

C5 convertase

74
Q

Regulation of Complement System

Properdin
• Protects _____ and stabilizes _______

A

C3b

C3 convertase

75
Q

Regulation of Complement System

FactorI
• Cleaves cell-bound or fluid phase _____________
•inactivates _____ and ——-

A

C3b and C4b

C3b and C4b

76
Q

Regulation of Complement System

Decay accelerating factor(DAF)

•is a _______ on surface of human cells
• Prevents ___________ or accelerates ________________ leading to ____________

• Acts on _______________ pathway

A

Glycoprotein

assembly of C3bBb

disassembly of preformed convertase

no formation of MAC

both classical and alternative

77
Q

Regulation of Complement System

C4b-bindingprotein(C4BP)

• Inhibits the action of C4b in ______ pathway
• Splits _______ and is a cofactor for ____

A

classical

C4 convertase

factor I

78
Q

Regulation of Complement System

ComplementReceptor1(CR-1)

• Co-factor for _____, together with _____

A

factor I

CD46

79
Q

Regulation of Complement System

Protectin and Vitronectin

• Inhibits _______ by binding _______

•Present on “______” cells to prevent ___________

A

formation of MAC

C5b678

self

complement from damaging them

80
Q

Protectin( ________)

Vitronectin( _______)

A

CD59

Sprotein

81
Q

_______(CD59)

________(Sprotein)

A

Protectin

Vitronectin

82
Q

Clinical Aspects of complement

  1. Deficiency of C5-C8 &Mannan-binding lectin
    • Predispose to _______ _______ _______
A

severe Neisseria bacteremia

83
Q

Clinical Aspects of complement

Deficiency of C3
• Severe, recurrent _________ and __________

A

pyogenic sinus & resp. tract infections

84
Q

Clinical Aspects of complement

Deficiency of C1 esterase inhibitor
• _____________ due to increased ————- and ________

A

Angioedema

capillary permeability and edema

85
Q

Clinical Aspects of complement

Deficiency of DAF

• Increased _________________ leading to ____________

A

complement-mediated hemolysis

paroxysmal nocturnal hemoglobinuria

86
Q

Clinical Aspects of complement

Transfusion mismatches
• Activation of complementgenerate
large amounts of anaphylatoxins & MAC
red cell hemolysis 6. Autoimmunediseases
• Immune complexes bind complement  low complement levels + activate inflammationtissue damage
7. Severeliverdisease
• Deficient complement proteins predispose to infection with pyogenic bacteria

A
87
Q

Clinical Aspects of complement

Transfusion mismatches

• Activation of complement generate
large amounts of anaphylatoxins & MAC leading to _______________

A

red cell hemolysis

88
Q

Clinical Aspects of complement

Autoimmunediseases
• Immune complexes bind complement leading to (low or high?) complement levels + activate _________ causing tissue damage

A

Low

inflammation

89
Q

Clinical Aspects of complement

Severe liver disease

• Deficient complement proteins predispose to ________ with _____

A

infection with pyogenic bacteria

90
Q

Clinical Aspects of complement

Factor I deficiency
• Low levels of ____ in plasma due to unregulated activation of _____ pathway leads to —————- in children

• Mutations in factor I gene has been implicated in development of ______________

A

C3

alternative

recurrent bacterial infections

Hemolytic Uremic Syndrome

House Clinical Pathology (45 decks)

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